Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Promoter methylation is an important mechanism of regulating E-cadherin expression. Methylation-specific PCR (MSP) assay was done to evaluate the promoter methylation status of E-cadherin gene in primary tumor samples from 23 cases of Chinese women with invasive ductal breast cancers. Western blotting assay was employed for E-cadherin and beta-actin expressions. Positive MSP results occurred in 26.1% (6/23) of primary tumor samples and none of four normal skin samples. These molecular events tended to occur in breast cancers associated with poor prognosis. Whereas the mean ratio of CDH1/beta-actin for six MSP-positive cases was 0.0290 +/- 0.0355, the mean ratio for 17 MSP-negative cases was 0.4726 +/- 0.5049 (P = 0.046). In conclusion, aberrant E-cadherin methylation preferentially occurs in invasive ductal breast cancer associated with poor prognosis and is one of the mechanisms of E-cadherin expression silence in breast cancers from Chinese women.
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PMID:E-cadherin promoter methylation can regulate its expression in invasive ductal breast cancer tissue in Chinese woman. 1212 60

Pituicytoma is a rare benign primary tumor of the neurohypophysis, occurring in the sellar and suprasellar spaces. We report here three new cases with immunohistochemical and electron microscopic study. Particular attention was paid to the expression of some cell adhesion molecules. These tumors were characterized by bundles of elongated cells strongly immunoreactive to anti-vimentin, S-100 protein, neural cell adhesion molecule and neuron-specific enolase antibodies. Glial fibrillary acidic protein (GFAP) was not recorded. It expressed the very late antigen alpha2 (VLAalpha2), but not VLAalpha5, and lacked epithelial markers expression (epithelial membrane antigen, E-cadherin), and specific neuronal markers (synaptophysin, chromogranin, neurofilament). Staining for pituitary hormones was negative. At the ultrastructural level, tumor/blood vessel basal lamina and cytoplasmic intermediate filaments were observed but desmosome or pericellular basal lamina were lacking. In one case few secretory granules were recorded. Differential diagnoses include granular cell tumors, pilocytic astrocytomas and spindle cell tumors such as solitary fibrous tumors, fibroblastic meningiomas and schwannomas. However, the unique pattern of antigenic expression and ultrastructural features of pituicytomas distinguish this rare tumor. As a subpopulation of pituicytes (which are distinctive glial cells of the neurophypophysis), some pituicytomas do not expressed GFAP. This suggests that pituicytomas presumably arise from pituicytes at various stages of their differentiation.
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PMID:Pituicytomas, a mis-diagnosed benign tumor of the neurohypophysis: report of three cases. 1217 18

The E-cadherin/catenin cell adhesion system is often down-regulated in epithelial tumors. This is thought to play an important role in cancer invasion and metastasis, and restoration of this system may suppress metastatic spread of cancer. In this study, the effects of a Ras farnesylation inhibitor (FTI-277) on E-cadherin-mediated cell-cell adhesion and metastatic potential were examined. In cell aggregation assays, FTI-277 stimulated aggregation of colon, liver and breast cancer cells. In vitro cultures of cancer cells showed that FTI-277 induced strong cell-cell contact. Immunoblotting analysis showed that FTI-277 increased E-cadherin/catenin (alpha, beta and gamma) expression and strongly stabilized E-cadherin/catenin with the actin cytoskeleton. Northern blotting studies indicated that the observed increase in the E-cadherin/catenin protein content was due to increased expression of their genes. After inoculation of the spleens of mice with severe combined immunodeficiency (SCID) with cancer cells, FTI-277 treatment for 3 weeks markedly reduced splenic primary tumor growth and the rate of liver metastasis compared with control counterparts. Our data demonstrate that FTI-277 can activate functioning of the E-cadherin-mediated cell adhesion system, which is associated with suppression of cancer cell metastasis. Therefore, selective inhibition of Ras activation may be useful for preventing cancer metastasis.
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PMID:Ras farnesylation inhibitor FTI-277 restores the E-cadherin/catenin cell adhesion system in human cancer cells and reduces cancer metastasis. 1235 56

We established a new lung cancer cell line, designated Y-ML-1B, from a lung cancer of a 70-year-old Japanese man with leukocytosis and thrombocytosis. Before surgical resection, the white blood cell and platelet counts were elevated to 34,400/mm3 and 668,000/mm3, respectively, and the granulocyte colony-stimulating factor (G-CSF) level in the serum was increased at 141 pg/mL. The primary tumor showed an undifferentiated morphology with large cells and induced extensive thickening of the pleura in the right hemithorax. The Y-ML-1B cells grow as a monolayer, with a doubling time of 19 hours, and are tumorigenic in nude mice, which showed a morphology similar to the primary tumor in xenografts. Analysis of the supernatant of cell culture medium of Y-ML-1B showed elevated levels of G-CSF and other cytokines such as interleukin (IL)-6, IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF), consistent with the high levels detected in the patient's serum. Cytogenetic analysis revealed aneuploidy of greater than 56 in metaphases with many structural abnormalities. Mutation analysis of the tumor suppressor genes showed that Y-ML-1B is inactivated in TP53 and RASSF1A, but not in p14(ARF), p16(INK4A), or RB. Neither activating mutations of KRAS or NRAS nor amplification of MYC or MDM2 were detected. Y-ML-1B expressed N-cadherin but not E-cadherin. This newly established cell line might serve as a useful model for studying the molecular pathogenesis for large cell cancers of the lung which express high levels of cytokines.
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PMID:Establishment of a large cell lung cancer cell line (Y-ML-1B) producing granulocyte colony-stimulating factor. 1237 11

The purpose of our study was to evaluate the frequency of hypermethylated tumor suppressor genes (TSGs) in peripheral blood, mouth and throat (M&T) rinsing fluid and nasopharyngeal (NP) swabs of nasopharyngeal carcinoma (NPC) patients. Six normal NP tissues, 43 M&T rinsing fluid, 37 NP swabs and 43 peripheral blood from healthy non-smokers and non-drinkers without a family history of NPC, and 30 NPC tumors and their matched body fluid were analyzed for the presence of hypermethylated p15, p16, Ras association domain family 1 (RASSF1A), E-cadherin, and death-associated protein kinase (DAPK) by methylation-specific PCR. Sequencing analysis was carried out on selected NPC tumors and body fluid samples. Twenty-nine (97%) tumors displayed methylation in at least 1 of the 5 genes. The methylation frequencies were 80% for p15, 77% for DAPK, 67% for RASSF1A, 53% for E-cadherin and 33% for p16. The frequency range of aberrant methylated genes in the body fluids were NP swabs (17-63%) and M&T rinsing fluid (17-50%). Methylation was found in <20% of peripheral blood for each respective gene. Methylation was, however, detected in 1 M&T rinsing fluid in which the primary tumor showed methylation free for RASSF1A. Five healthy individuals exhibited methylation for DAPK, or RASSF1A, or p15 in their body fluid samples. All body fluid samples of healthy controls showed methylation free for E-cadherin and p16. Epigenetic change is found frequently in NPC and the high detection rate in body fluids suggest its potential application in non-invasive screening of NPC or detection of residual carcinoma after treatment.
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PMID:Evaluation of hypermethylated tumor suppressor genes as tumor markers in mouth and throat rinsing fluid, nasopharyngeal swab and peripheral blood of nasopharygeal carcinoma patient. 1276 73

Dysadherin is a cancer-associated cell membrane glycoprotein. Its cDNA encodes 178 amino acids, including a putative signal sequence, a potential O-glycosylated extracellular domain, a single transmembrane domain, and a short cytoplasmic tail. Dysadherin is believed to down-regulate the expression of E-cadherin, the prime mediator of cell-cell adhesion in epithelial cells, by a posttranscriptional mechanism and promote the metastasis of carcinoma cells. To evaluate the association between dysadherin expression and E-cadherin expression in thyroid carcinoma, immunostaining for dysadherin and E-cadherin was performed in 51 papillary, 10 follicular, and 31 undifferentiated carcinomas. Immunoreactivity for dysadherin, localized at cell-cell boundaries, was detected in 39 of the 51 papillary carcinomas and all 31 undifferentiated carcinomas but not in the follicular carcinomas or normal thyroid tissue controls. Dysadherin expression was significantly higher in undifferentiated carcinoma than in papillary carcinoma and follicular carcinoma and showed significant negative correlation with E-cadherin expression. The degree of dysadherin expression was significantly associated with the prognosis, occurrence of secondary undifferentiated carcinomas, size of the primary tumor, and metastasis to the regional lymph nodes and lungs. In conclusion, a process involving increased dysadherin expression may lead to an adverse clinical outcome.
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PMID:Dysadherin: expression and clinical significance in thyroid carcinoma. 1297 Mar 17

A new cell line of human uterine endometrial undifferentiated carcinoma, designated as TMG-L, was established from the metastatic lymph node of 56-year-old patient TMG-L cells have been cultured with Ham's F-12 medium supplemented with 10% FCS and grew as a loosely adherent monolayer with polygonal or spindle-shaped cells exhibiting poor cell-cell contact and piled up against each other, showing a tendency to grow as floating cells. The doubling time of this cell line was about 48 hours, and chromosomal analysis revealed aneuploidy at passage 25. The cells formed tumors in SCID mouse, the histology of which was similar to that of undifferentiated carcinoma component of primary tumor. TMG-L cells showed the loss of expression and membranous localization of either E-cadherin or alpha-catenin, implied corresponding loss of their adhesive function. And this dysfunction implicated the biological aggressive behavior of uterine endometrial undifferentiated carcinoma. This cell line appears to provide a useful system for studying uterine undifferentiated carcinoma in vivo and in vitro.
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PMID:Establishment and characterization of a human uterine endometrial undifferentiated carcinoma cell line, TMG-L. 1297 23

Seprase is a cell surface serine protease that is expressed to high levels by infiltrating ductal carcinomas of the breast but its function in malignancy is unknown. MDA-MB-435 (WT435) and MDA-MB-436 (WT436) human breast cancer cells express high levels of seprase as do the carcinoma cells in tumors of human breast cancer patients. To investigate its role in the pathobiology of breast cancer, seprase was specifically reduced in WT436 and WT435 cells by expression of antisense seprase cDNA. Decreased expression of seprase was confirmed in the antisense transfectants by zymography, immunoblotting, and fluorescence-activated cell sorting of cells labeled with antibody to seprase. Control-transfectants continued to express high levels of seprase. Seprase-deficient cells growing on type I collagen gels reveal a markedly different morphology than the parental or control-transfected cells that express high levels of seprase. The seprase-deficient cells grow in islands and aggregates of tightly attached cells while cells with high seprase expression grow as groups of separate individual cells. Interestingly, the aggregated growth of the seprase-deficient cells was not correlated with increased expression of E-cadherin. Seprase-deficient breast cancer cells also exhibit altered growth properties. Seprase-deficient cells and those with high seprase levels proliferate in serum-containing media. However, in serum-free medium seprase-deficient cells proliferate much more slowly than their seprase-expressing counterparts. These findings indicate that seprase promotes the aberrant growth of breast cancer cells by reducing their dependence on exogenous growth factors. Seprase may contribute to the pathogenesis of breast cancer by promoting growth of the primary tumor and by facilitating the growth of breast cancer cells in metastases at other sites of the body.
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PMID:Seprase, a membrane-bound protease, alleviates the serum growth requirement of human breast cancer cells. 1452 36

Carcinoembryonic antigen (CEA) has been suggested as a metastatic activator in colorectal carcinoma, whereas the E-cadherin expression is downregulated in a variety of carcinomas. CEA and E-cadherin expressions were simultaneously assessed with regard to tumor progression in the various sites of colorectal carcinomas with liver metastasis. Twenty-six consecutive patients who had colorectal carcinoma with liver metastasis underwent curative surgery for primary tumor and liver metastasis. CEA and E-cadherin expression were identified on immunohistochemical staining using the labeled streptavidin-biotin method. Their mRNA expression was also detected by RT in situ PCR using one-step reverse transcription-polymerase chain reaction (RT-PCR). CEA and E-cadherin expression scores in the tumor center were greater than those in the tumor margin in both primary tumor and liver metastasis (P<0.001 to 0.006). CEA expression scores were closely associated with E-cadherin expression scores on the corresponding tumor site (P<0.001 to 0.017). CEA and E-cadherin mRNA expression was greatest in the hepatocytes adjacent to liver metastasis, next greatest in the primary tumor, and least in the liver metastasis (P<0.001 to 0.002). CEA mRNA expression was also closely correlated with E-cadherin mRNA expression in the primary tumor (P<0.001) and in the adjacent hepatocytes of the liver metastasis (P=0.018). Patients with a lesser CEA expression score in the liver metastasis margin appeared to have a longer disease-free survival period than did those with a greater CEA expression score. Expression of CEA and E-cadherin was closely correlated with the mRNA levels. Furthermore, these correlations may be implicated in the tumor progression of colorectal carcinoma considering their biological properties.
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PMID:Coexpression of carcinoembryonic antigen and E-cadherin in colorectal adenocarcinoma with liver metastasis. 1459 71

This study was conducted to clarify the relationship between E-cadherin expression on tumor and lymph node metastasis as well as its prognostic roles in resected non-small-cell lung cancer. Two hundred forty-nine patients, who underwent surgical resection (stage I-IIIA), were examined. Paraffin-embedded sections of the primary tumors in all cases and of the metastatic lymph nodes in stage IIIA disease were stained with a monoclonal antibody against E-cadherin. Decreased expression of E-cadherin correlated with pathologic stage, tumor size, lymph node metastasis, and histological grade. The 5-year survival rate of E-cadherin-negative patients with stage IIIA disease was significantly lower than that of E-cadherin-positive patients. Multivariate analysis in stage IIIA disease indicated that E-cadherin was an independent prognostic factor. In the patients with clinical N0 tumors, the frequency of pathological N2 tumors was significantly higher in cases where the primary tumor was recognized as E-cadherin expression negative than in cases where the primary tumor was recognized as positive. Decreased E-cadherin expression showed correlation with presence of lymph node metastasis in resected non-small-cell lung cancer and with the prognosis of patients with stage IIIA disease.
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PMID:Expression of E-cadherin and lymph node metastasis in resected non-small-cell lung cancer. 1465 29


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